Know the Risks: Lifestyle

Management of Dyslipidemia
by Paul Sorace, M.S., CSCS, Thomas LaFontaine, Ph.D., FACSM, CSCS, NSCA-CPT,
and Tom R. Thomas, Ph.D.

Learning Objectives Dyslipidemia is caused by genetic and environmental

To present an overview of dyslipidemia, postprandial factors that lead to problems with enzyme deficiencies,
lipemia, and the evidence of how effective lifestyle apolipoproteins, or lipoprotein particles. There are a number
management can be used for improving and/or preventing of factors that contribute to dyslipidemia (see Table 2
dyslipidemia and to provide evidence-based exercise for a partial listing).
activity guidelines. Dyslipidemia also is a characteristic of the recently
defined metabolic syndrome. The metabolic syndrome
Key words: Cholesterol, Dyslipidemia, Postprandial consists of a group of coronary heart disease (CHD) risk
Lipemia, Exercise, Physical Fitness. factors which includes glucose intolerance (fasting plasma
glucose of 100–125 mg/dL), atherogenic dyslipidemia
(TGs 150mg/dL and HDL cholesterol <40 mg/dL in
Dyslipidemia
Abnormal blood lipids, known as dyslipidemia, are an Table 1. Cholesterol Guidelines Based on the
increasing health problem in the United States and the National Cholesterol Education Program Adult
world. Approximately 107 million American adults have Treatment Panel
borderline or high total cholesterol (1) (see Table 1 for Total Cholesterol
cholesterol guidelines). Dyslipidemia is one of the major risk Desirable <200 mg/dL
factors for heart disease (1–4). Excess cholesterol builds up
Borderline 200–239 mg/dL
in the walls of the arteries. Over time, this buildup
contributes to atherosclerosis, a disease process in which High 240 mg/dL
arteries become narrowed and blood flow is impaired. If the LDL Cholesterol
blood supply to a portion of the heart is completely cut Optimal <100 mg/dL
off by a blockage, the result is a heart attack. Near optimal 100–129 mg/dL
There are a number of different forms of dyslipidemia. Borderline high 130–159 mg/dL
Hypercholesterolemia indicates elevated blood cholesterol
High 160–189 mg/dL
levels (2). Hypertriglyceridemia implies elevated
Very high 190 mg/dL
triglycerides (TGs). Hyperlipidemia indicates elevated
cholesterol and TGs. Hyperlipoproteinemia is defined as HDL Cholesterol
elevated lipoproteins (2). Hypoalphalipoprotein syndrome High 60 mg/dL
denotes low high-density lipoprotein (HDL) cholesterol (2). Low <40 mg/dL
Postprandial lipemia (PPL), discussed in greater detail Triglycerides
later, is characterized by a postprandial rise in TG-rich Normal <150 mg/dL
lipoproteins after eating.
Borderline high 150–199 mg/dL
One of the first steps in atherogenesis is the infiltration
and entrapment of low-density lipoproteins (LDLs) in High 200–499 mg/dL
the blood vessel wall. This leads to a series of events Very high 500 mg/dL
(e.g., oxidation of LDLs, monocyte migration, macrophage For persons with a very high risk, their LDL cholesterol goal will be
uptake of modified LDLs, foam cells, fatty streaks, etc.) <70 mg/dL (6).
Reference: http://www.nhlbi.nih.gov/guidelines/cholesterol/atp3_rpt.htm.
that result in the development of fibrous plaques within LDL indicates low-density lipoprotein; HDL, high-density lipoprotein.
the walls of the intima.

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 LIFESTYLE MANAGEMENT OF DYSLIPIDEMIA

Table 2. Causative Factors for Dyslipidemia

 Heredity/Genetics
 Advanced age
 Gender (women generally have lower total cholesterol
levels than men of the same age before menopause)
 Cigarette smoking
 Excessive alcohol consumption (>1 drink/day in women
and >2 in men)
 Diet high in saturated fats, trans-fatty acids, and
cholesterol and diet low in fiber
 Physical inactivity
 Overweight or obesity (especially abdominal obesity)
 Certain medications (e.g., beta blockers, thiazide diuretics)
 Anabolic steroids
do not mix, the body combines protein plus lipid so that
the lipid substance can be transported in plasma. There
 Diabetes mellitus
are several lipoproteins in the body, with different functions
 Hypothyroidism (see Table 3). Some contribute to cardiovascular disease
 Menopause (e.g., LDLs) and some help prevent it (e.g., HDLs).
In summary, dyslipidemia refers to an abnormality of
lipoproteins, covering a variety of disorders relating to
men and <50 mg/dL in women), increased blood abnormal levels of total cholesterol, LDL cholesterol,
pressure (130/85 mm Hg), abdominal obesity (waist HDL cholesterol, and/or TGs.
circumference of 102 cm or greater in men and 88 cm
or greater in women), a prothrombotic state, and a Postprandial Lipemia
proinflammatory state (5). A prothrombotic state is a Postprandial lipemia (PPL) refers to the rise in TG-rich
condition that predisposes to venous or arterial thrombosis. lipoproteins (e.g., very low density lipoproteins [VLDLs])
A proinflammatory state is the presence of low-grade after a meal. It is a dynamic condition in which humans
generalized inflammation within the body that increases spend the majority of their time (7). PPL reflects a
cardiac risk. combined measure of an individual’s capacity to metabolize
Lipoproteins are the carriers of lipids (primarily TGs. Elevated/prolonged PPL, defined as a delayed
cholesterol and TGs) in the blood. Because fat and water clearance of TGs after a high-fat meal, is a significant

Table 3. Cholesterol/Lipoprotein Classes

Total Cholesterol: This represents the total serum cholesterol.
Triglycerides (TGs): Lipids carried through the bloodstream to tissues. Most of the body’s fat tissue is in the form of
triglycerides, stored for use as energy. Triglycerides are obtained primarily from fat in foods.
Chylomicrons: A small fat globule composed of protein and lipid (fat). Chylomicrons are found in the blood and lymphatic
fluid where they serve to transport fat from its port of entry in the intestine to the liver and to adipose tissue.
Very low density lipoproteins (VLDLs): Lipoproteins that are rich in triglycerides, produced in the liver, and are the major
carriers of endogenous (produced by the body) triglycerides
Low-density lipoproteins (LDL): The final-stage lipoprotein from the catabolism of VLDLs. LDLs is the primary carrier of
cholesterol in the body. Intermediate density lipoproteins (IDL) are a subfraction of LDLs. LDLs are commonly known
as the ‘‘bad’’ cholesterol because they contribute to the buildup of plaque within the arteries. There are 7 different sizes
of LDLs. The smaller, denser LDLs are more atherogenic.
High-density lipoproteins (HDL): HDLs are composed of a high proportion of protein with little triglyceride and
cholesterol. HDLs are involved in reverse cholesterol transport, which is believed to protect against heart disease and
stroke. HDLs are commonly known as the ‘‘good’’ cholesterol because they help keep cholesterol from building up in
the arteries. There are different subfractions of HDLs: HDL2 and HDL3. HDL2 is the subfraction that appears to be
protective against heart disease.

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 LIFESTYLE MANAGEMENT OF DYSLIPIDEMIA

risk factor for the development of atherosclerosis (7, 8).

Table 4. Lipid Enzymes
The exchange of core lipids between postprandial
lipoproteins and LDLs/HDLs increases during prolonged Lipoprotein Lipase (LPL)—Endothelial-anchored enzyme
PPL in susceptible persons, resulting in elevated TGs; primarily responsible for hydrolysis (breakdown) of
chylomicrons and very LDL triglycerides, especially in
the production of small, dense LDL particles; and muscle and adipose tissue
reduced HDLs (7). Smaller, denser LDLs are more Lecithin-Cholesterol Acyltransferase—Enzyme that
atherogenic than the larger, less dense LDLs. Other converts free cholesterol to cholesteryl ester on HDL
atherogenic factors including clotting factors, platelet (reverse cholesterol transport). It also is involved in the
reactivity, and monocyte and cytokine expression, all of conversion of HDL3 to HDL2.
which contribute to endothelial dysfunction, may increase Cholesterol Ester Transport Protein—Protein that
transfers lipids among lipoproteins, especially cholesteryl
during PPL (7). ester from HDL to very LDL, in exchange for
Testing for PPL involves a 12-hour fast and initial triglycerides
blood collection. Subjects then ingest a high-fat beverage, Hepatic Lipase—Endothelial-anchored enzyme in the
and blood samples are collected every 2 hours for 8 hours. liver that is primarily responsible for hydrolysis of
Triglyceride concentrations are measured by colorimetry triglycerides and phospholipids (lipids with a phosphate
group in place of one of the three fatty acid chains) in
(quantitative chemical analysis by color), and values IDLs and HDLs
are plotted over time. PPL is assessed using total area
Triglyceride Lipase—The enzyme that catalyzes the
under the curve (AUC). A large value for TG area AUC hydrolysis (breakdown) of triglycerides in the fat cells of
indicates that the TGs were maintained in the blood longer adipose tissue, releasing free fatty acids and glycerol into
than expected. the bloodstream. It is inhibited by insulin and activated
by glucagon and adrenaline.
Exercise Effects on Lipid Metabolism HMG-CoA Reductase—The first enzyme of the
HMG-CoA reductase pathway, the metabolic pathway
The lowering of TGs is the most consistent effect exercise that produces cholesterol and various other biomolecules
has on lipoproteins. HDLs often are increased with
sustained aerobic exercise that results in an expenditure
of >1,200 calories/week, but this effect is less consistent
and may be genetically predetermined (9). The greater increases hepatic HDL production and the conversion
the exercise volume (and caloric expenditure), the more of HDL3 to HDL2 in the blood, both of which protect
likely an exerciser will achieve a significant increase against heart disease (3).
in HDL cholesterol. Lower TGs are typically observed The evidence for exercise alone reducing LDLs and
with both acute exercise and sustained aerobic exercise total cholesterol is less conclusive. It appears that weight
training (3). TGs are used as energy by skeletal muscles loss/fat loss is required for significant reductions in LDLs
during endurance exercise. The enzyme lipoprotein lipase and total cholesterol (3, 10). Regular aerobic exercise does,
(LPL) splits TGs from VLDLs, making them available for however, produce favorable changes in LDL subfractions,
uptake by skeletal muscles. Chronic exercise training also which will reduce the risk of CHD. For example, aerobic
exercise has been shown to convert smaller LDLs to larger
LDLs, reducing cardiac risk (3, 11).
Exercise training also favorably alters lipid enzyme
activity, resulting in improved lipid profiles. Table 4
lists and defines the major enzymes involved in lipid
metabolism. LPL and lecithin-cholesterol acyltransferase
are increased with aerobic exercise, whereas hepatic
lipase is usually decreased (3). The effects of exercise
training on cholesterol ester transport protein are
inconclusive at this time (3). Genetic deficiencies can
alter the exercise response for some individuals.
For example, LPL activity will not be increased in
those who have a LPL deficiency (2). It was recently
demonstrated in 35 pairs of monozygotic twins (active
twins ran a mean of 63 km/week vs. a mean of
ACSM Photo/Adrienne D. Porter 7 km/week in the inactive twins) that low HDL

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 LIFESTYLE MANAGEMENT OF DYSLIPIDEMIA

energy expenditures are recommended to produce notable

changes in individuals with dyslipidemia (3, 4, 10).
Cross-sectional studies have shown that lipids continue to
improve across weekly running distances from <10 to >40
miles in a direct dose-response relationship (13).
The effect of exercise on PPL also is significant.
Individuals who regularly perform aerobic exercise typically
display low levels of PPL (14). Vigorous aerobic exercise
has been shown to reduce PPL in men with elevated
TGs, even when performed 12 hours before a high-fat
meal (15). In a recent study, intermittent exercise in young,
normolipidemic men and women was shown to improve
PPL significantly more than continuous exercise (16).
The breakdown of blood TGs (and some TG-rich
lipoproteins) is increased during exercise and continues
well into the recovery phase. Exercise that stimulates fat
use as a substrate during and after the activity helps clear
TG from the blood. In addition, exercise stimulates the
enzyme LPL and this enzyme may remain active for
several hours. Thus, moderate intensity exercise attenuates
PPL (17, 18). It is important to note that the favorable
effects (e.g., TG lowering) of endurance exercise on
PPL seem to be a result of acute metabolic changes as
opposed to chronic exercise effects (14, 15). This encourages
daily or near daily aerobic exercise to treat elevated PPL.
Possible mechanisms for the exercise-induced TG
reductions include increased muscle LPL activity and
reduced hepatic TG secretion (14, 17).
There only have been a couple of studies on resistance
training and PPL, and the results were inconsistent (19, 20).
cholesterol may be largely determined by genetic factors Thus, there are no specific guidelines to recommend at
and is less effectively treated with vigorous exercise (12). the present time.
Weight loss is another lifestyle factor that significantly
improves dyslipidemia. Obesity typically elevates VLDL
Lifestyle Effects on Dyslipidemia and LDL fractions, increases TG levels, lowers HDL
National Cholesterol Education Program III recommends cholesterol, increases blood pressure, and promotes insulin
nutritional intervention, increased exercise/physical resistance. Weight loss typically lowers LDLs, TGs, and
activity, and weight loss for many individuals with total cholesterol (2, 3). HDLs may increase, decrease,
dyslipidemia (5). There is substantial evidence to support or remain the same (2, 3). If weight loss is combined
the profound beneficial effects of lifestyle changes on with aerobic exercise, HDLs are more likely to be
dyslipidemia (3, 4, 10, 11). Although there are a number sustained or increase following training. Weight loss also
of medications (e.g., statins) that are effective for treating lowers blood pressure, improves glycemic control, and
dyslipidemia, lifestyle changes alone can often normalize reduces inflammation linked to metabolic and cardiac
lipid profiles. Lipid lowering typically results in modest diseases (3, 5, 21, 22).
plaque regression and stabilization, reducing the risk Exercise training can improve lipid profiles either directly
of a cardiac event (3). (without weight loss) by increased lipid enzymatic activity
Regular aerobic exercise is an essential lifestyle or indirectly (reduced body weight) (2). When weight
component for improving/controlling blood lipids. loss occurs in conjunction with exercise, LDL and total
The total amount of physical activity seems to be more cholesterol are usually lowered (2, 3). Weight loss also
important than the intensity to induce beneficial effects has beneficial effects on lowering PPL, as obesity increases
on lipoproteins (10, 11). Significant daily and weekly PPL. When weight loss is indicated, a loss of 5% to

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10% body weight from baseline is a starting goal (4). remember that lifestyle physical activity (e.g., climbing
This amount of weight loss can significantly improve stairs, lunchtime walks, housework) contributes to the
blood lipids. However, even when there is minimal or total weekly energy expenditure. Also, for a well-rounded
no weight loss, an improved lipid profile can still be exercise program, resistance and flexibility training should
achieved with adequate exercise (11). be incorporated (see Table 5 for guidelines).

Exercise/Physical Activity Guidelines Nutritional Guidelines

It is prudent that the fitness professional check with the Dietary modification is a powerful nonpharmacological
individual’s physician if he or she is taking lipid-lowering strategy for improving blood lipids. Diets that are high in
medications or other medications for any coexisting diseases saturated and trans-fat and cholesterol increase TGs, LDL,
(e.g., obesity, hypertension, type 2 diabetes) that may and total blood cholesterol. Polyunsaturated fats (e.g., corn
require medical clearance. Statins, for example, can oil) seem to have a neutral effect on blood cholesterol,
cause muscle damage (myopathy) and this should be whereas monounsaturated fats (e.g., olive oil) seem to
considered (4). Table 5 summarizes general exercise sustain HDLs and lower LDLs and TGs. Reducing
guidelines for dyslipidemia. The emphasis should be on saturated and trans-fats and cholesterol intake will usually
aerobic exercise and total weekly caloric expenditure. improve blood lipids. Even though there is variability
A good initial goal is to perform aerobic exercise three in individual responses to dietary changes, reducing total
to five times per week for 20 to 60 minutes, expending calories consumed, particularly saturated fat calories,
1,200 calories/week. Ideally, aerobic exercise for which results in weight loss, typically lowers total and
dyslipidemia should gradually progress, as tolerated, LDL cholesterol. HDL cholesterol is sometimes lowered
to five to seven times per week for 40 to 60 minutes, as well, but when dieting is coupled with exercise, HDL
creating an energy expenditure of >2,000 calories/week (4). cholesterol can be maintained (2, 3, 23, 24).
A gradual increase in aerobic exercise intensity should High-carbohydrate diets can increase TG levels and
also occur. Exercise programs with higher volumes and decrease HDL cholesterol, but again, this effect is negated
intensities have been shown to be most effective for with aerobic exercise (2, 3, 23, 24). Dietary fiber, particularly
increasing HDL cholesterol (11). These guidelines may soluble fiber, helps to lower blood cholesterol levels.
also need adjusting based on coexisting diseases, current Omega-3 fatty acids lower blood TG levels (3). Plant
fitness level, and time constraints that may be present. sterols also have been shown to favorably alter lipid profiles,
The aerobic training may need to be performed particularly when combined with aerobic exercise (25).
intermittently throughout the day. It is important to Moderate alcohol consumption (no more than one drink per

Table 5. Summary Exercise Programming

Components of Frequency,
Training Program (session
week 1) Intensity Duration Activity
1
Cardiorespiratory 3–5 days
week 40%/50%–85% 20–60 min large muscle groups
HRR or VO2R dynamic activity
55%/65%–90% HRmax
12–16 RPE
1
Resistance 2–3 days
week volitional fatigue (MMF) 1 set of 3–20 repetitions 8–10 exercises
(e.g., 19–20 RPE) (e.g., 3-5, 8–10, 12–15) include all major
muscle groups
or
stop 2–3 repetitions
before volitional
fatigue (e.g., 16 RPE)
Flexibility minimal 2–3 stretch to tightness at the 15–30 seconds static stretch all major
days
week 1 end of the range of 2–4 times/stretch muscle groups
ideal 5–7 motion but not to pain
days
week 1

HRR indicates heart rate reserve; MMF, momentary muscular fatigue; RPE, rating of perceived exertion; VO2R, maximal oxygen uptake reserve.

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day in women and lighter persons and no more than two

drinks per day in most men) (4) may raise HDL cholesterol
levels. It may also increase TGs, but its effect on LDL
cholesterol appears to be minimal.
Table 6 summarizes the key components of a diet to
help lower blood lipids. The emphasis should be on
restricting fat, particularly saturated fats, and cholesterol
intake while increasing intake of soluble fiber and other
foods such as soy, almonds, walnuts, plant sterols and
stanols, cold water fish (e.g., salmon), etc., which have
been shown to have a beneficial effect on blood lipids.
Here are some nutrition tips that favorably help impact
blood lipids:
 Eat fish two to three times per week. The fish should
be baked, not fried.
 Use healthy oils for cooking, such as olive oil and
walnut oil.
 Eat whole grain products. Avoid or limit starchy white
pasta and bread.
 Add or increase oats and oatmeal intake.
 Increase consumption of green vegetables. Broccoli,
spinach, lettuce, and green beans are all examples
of healthy carbohydrate, low-calorie green vegetables.
 Eat whole fruits and berries.
 Avoid/reduce rich, fattening desserts.
 The amount of each type of fiber varies in different plant
foods. To receive the greatest health benefit, eat a wide
variety of high-fiber foods.
fitness, he was found to have had a recent surgical repair
Case Study of a left quadriceps muscle rupture and had gained 45 lbs over
In December of 2003, a 75-year-old man was referred for six to eight months of recovery and rehabilitation. He had a
lifestyle management to lose body weight and manage history of dyslipidemia and overweight but was not diabetic
cardiovascular risk factors. On medical history and physical nor hypertensive. He was a nonsmoker, and his mother and
father died of cardiovascular disease at age 78 and 84,
Table 6. Healthy Dietary Guidelines for Improving respectively. He has been an avid golfer since retirement in
Blood Lipids 1995, walking nine holes, three days/week. He also has been
Total calories: Enough to support energy needs, yet very active in his daily life but had not been following a regular
allowing for a 5%–10% body-weight loss, if indicated exercise program. His dyslipidemia was being treated only with
Fat consumption: 20% total calories Altaprev, 20 mg/day, started in April of 2001. He had had no
advice in regard to weight loss, exercise, or other therapeutic
Saturated fat consumption: 7% total calories
lifestyle changes. He was enrolled in the INTERXVENTUSA
Cholesterol consumption: 100–150 mg/day
Cardiovascular Risk Reduction Program (www.
Fiber consumption: 25–40 g/day interventusa.com). After one year, he had lost 43 lbs
Soluble fiber consumption: 10–15 g/day (from 244 to 201 lbs). He was eating a low-fat, high-fiber
Protein intake: 15% total calories, emphasizing vegetable diet (22% fat calories and 45 g of fiber per day by seven day
proteins food recall) and exercising 260 minutes/week on average
Carbohydrate intake: 60%–65% total calories, (walking 200 minutes and Airdyne bicycle ergometer
emphasizing complex forms 60 minutes). Lipid changes with indicated therapy from
04/01 through 01/05 are summarized below:

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Total Cholesterol
Altaprev Dosage (TC) Triglycerides LDL HDL
and/or Lifestyle Body Weight,
Date Therapy (LT)* (all data in mg/dL except TC/HDL Ratio) TC/HDL lbs
Pre-lifestyle therapy*
4/01 On Altaprev, 282 177 191 56 5.04 238
20 mg/day
No LT*
12/03 20 mg/day 222 158 134 54 4.11 244
Altaprev
Started LT* 12/03
Post-lifestyle therapy*
08/04 20 mg/day + LT* 146 104 67 58 2.52 219
Altaprev decreased
to 5 mg/day
01/05 5 mg/day 172 90 88 66 2.61 201
Altaprev + LT*
*Lifestyle therapy included exercise training at 260 minutes/week, 22% fat, 45 g fiber per day, and progressive weight loss as described in table.

Summary youth. He is a fellow of the American College of Sports

Dyslipidemia is a condition that promotes the genesis and Medicine and a former member of the ACSM Registered
progression of atherosclerosis. Dyslipidemia and PPL can Clinical Exercise Physiologist Practice Board. He is ACSM
often be prevented or treated with lifestyle management Registered Clinical Exercise Physiologist1 certified. Dr.
of exercise/physical activity, proper nutrition, and weight LaFontaine has more than 30 years of clinical experience in
loss (if needed). Having a sound knowledge of lipid health and fitness promotion and education and in primary
disorders, their associated risks, guidelines for treatment, and secondary disease prevention programs.
and understanding how lifestyle management can prevent/
improve dyslipidemia will better enable the fitness Tom Thomas, Ph.D., is currently a professor
professional to coach individuals to live healthier lives. in the Department of Nutritional Sciences
and director of the Exercise Physiology
Paul Sorace, M.S., CSCS, is the clinical Program at the University of Missouri.
exercise physiologist at the Center for He has been a member of the American
Allergy, Asthma, & Immune Disorders at College of Sports Medicine for 34 years.
Hackensack University Medical Center in His current research interests include exercise
Hackensack, NJ. He conducts fitness and the metabolic syndrome, and exercise and weight
seminars throughout the East Coast and is loss/regain.
a member of the ACSM Registered Clinical
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